Acute Pancreatitis
Acute pancreatitis is a relatively common condition presenting with severe, acute, constant epigastric pain. Incidence of ~5 per 100,000/year. Acute pancreatitis has a significant mortality. Early complications include acute renal failure, DIC, hypocalcemia and ARDS. Treatment of pancreatitis is mainly supportive and includes “pancreatic rest”. Withholding food or liquids by mouth until symptoms subside, and adequate narcotic analgesia. At the core surgical training interview clinical station you may be asked how you would assess and manage a patient presenting with acute epigastric pain.
Pathology:
Inflammation of the pancreas with release of inflammatory cytokines and pancreatic enzymes. Acute pancreatitis is an acute inflammatory process caused by the effects of enzymes released from the pancreatic acini.
Differential Diagnosis
- Peptic Ulcer disease
- Intestinal Obstruction
- Triple A (AAA)
- Gall stone disease
- Viral gastroenteritis
- Myocardial Infarction
Aetiology:
‘GET SMASHED’
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion stings
Hyperthermia, Hyperlipidaemia
ERCP
Drugs: NSAIDs, Thiazide diuretics, Azathioprine, Isoniazid
Pathogenesis
Duct obstruction: may lead to reflux of bile into the pancreatic ducts causing injury; increased intraductal pressure may damage pancreatic acini, leading to leakage of pancreatic enzymes with further damage to pancreas.
Direct acinar damage: due to viruses, bacteria, drugs or trauma. Protease release causes widespread destruction of pancreas and increases further enzyme release with consequent further damage.
Lipase causes fat necrosis, resulting in characteristic yellowish-white flecks on the pancreas, mesentery and omentum, often with calcium deposition (fat necrosis).
Elastase destroys blood vessels, leading to haemorrhage within the pancreas and haemorrhagic exudate into the peritoneum.
Haemorrhage may be extensive, leading to acute haemorrhagic pancreatitis.
Biochemical Changes
Increased serum amylase: released from damaged acini into bloodstream.
Hypocalcaemia: arises because of deposition of calcium in areas of fat necrosis.
Hyperglycaemia: occurs because of associated damage to pancreatic islets.
Abnormal liver function tests, especially raised bilirubin and alkaline phosphatase, due to mild obstruction of bile ducts by oedema.
Symptoms:
Epigastric pain radiating to back, relieved sitting forward,
Nausea,
Vomiting
Signs:
Epigastric tenderness and guarding, septic shock
Cullen’s Sign: Periumbilical bruising
Grey-Turner’s Sign: Bilateral flank bruising indicates pancreatic necrosis with
retroperitoneal bleeding
Investigations:
Bloods: FBC, U&E, LFTs, serum amylase >1000Iu/mL, lipase, blood gas
Imaging: Abdominal X-Ray - loss of psoas shadow indicates retroperitoneal fluid
Ultrasound Abdomen: gallstones, pancreatic fluid
CT Abdomen: pancreatic inflammation, fluid
Treatment:
Medical: IV fluids, oxygen, analgesia and assess severity
If severe, transfer to HDU/ITU for monitoring of vital signs and fluid balance with nutritional support
Complications:
Pancreatic pseudocyst or necrosis,
Chronic pancreatitis,
ARDS,
SIRS,
Death
Prognosis:
Several classification systems for severity Modified Glasgow, Ranson and APACHE II
Modified Glasgow Scoring For Pancreatitis:
Mnemonic – ‘PANCREAS’
3 or more criteria in first 48 hours indicates a severe attack
PaO2 <8KPa
Age >55 years
Neutrophils >15x109/L
Calcium <2mmol/L
Renal Function Urea >16mmol/L
Enzymes LDH >600IU/L or AST >2000IU/L
Albumin <32g/L
Sugar >10mmol/L
Mortality
Overall mortality is 10–20%
Severe haemorrhagic pancreatitis has mortality rate of 50%.
The Usual cause of mortality is multiple organ failure.
